( Tischler et al . 2017 ).
Activation of TERT as a result of promoter mutations (specifically, chr5:1295228C > T and chr5:1295250C > T) were initially found in melanoma ( Horn et al . 2013 ) and have subsequently been shown to be one of the most

telomerase reverse transcriptase (TERT), a catalytic subunit of the telomerase enzyme complex. As the de-repression of TERT gene transcription is intimately coupled with the acquisition of telomerase activity in transformed cells, regulatory mechanisms

transcriptase ( TERT ) gene, which encodes for the catalytic subunit of telomerase, is implicated in tumorigenesis and cell immortalization. The two promoter mutations C228T and C250T were recently reported in human melanomas and other human cancer types

Introduction
Telomerase reverse transcriptase ( TERT ) has a canonical role maintaining telomere length and the nontelomeric function, which can regulate the expression of various genes involved in cell proliferation and cellular signaling

frequency of PD-L1 expression in various thyroid cancers and the relationship between PD-L1 expression and clinicopathologic factors including BRAF , TERT promoter status and disease progression were evaluated.
Materials and methods
Case

Rengyun Liu and Mingzhao Xing

required to achieve this. Two recently discovered mutations in the promoter of the gene for telomerase reverse transcriptase (TERT) in thyroid cancer show promise in this regard – chr5:1 295 228C>T and chr5:1 295 250C>T (termed herein as C228T and C250T